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Letters to the Editor |
Uniformed Services University of the Health Sciences, (D.F.S., S.Q.D.), Bethesda, Maryland; Kyoto University Graduate School of Medicine (T.A.), Kyoto, Japan; and Hyogo Prefecutural Amagasaki Hospital (H.K.), Hyogo, Japan
Address correspondence to: Donald F. Sellitti, Ph.D., Department of Medicine, Division of Endocrinology, Uniformed Services University of the Health Sciences, Room A 3060, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799.
To the editor:
Busuttil and Frauman (1) have recently studied the expression of the TSH receptor (TSH-R) in all four chambers of the human heart, and have failed to confirm using RT-PCR earlier findings of TSH-R transcript in this organ (2, 3). We suggest that this report, rather than confirming an absence of TSH-R in the heart, is better interpreted as supporting a scarcity of the transcript in cardiac muscle per se. In our earlier report of TSH-R expression in the porcine heart (4), we did detect TSH-R transcript by RT-PCR with primers spanning exons 9 and 10 of the full-length receptor, but expression levels varied regionally. Although essentially undetectable by single-round PCR in the left ventricular myocardium and in purified ventricular cardiocytes (in support of the study by Busuttil and Frauman), definitive TSH-R expression was observed in the right atrium and in purified atrial cardiocytes. However, the highest expression levels were observed in isolated coronary arteries and in epicardial adipose tissue, neither of which was examined in the study of human cardiac tissues (1). All PCR products in our study were confirmed as TSH-R by DNA sequencing. The differential pattern of expression of TSH-R in porcine cardiac tissues and its reproducibility in two different pig hearts argues strongly against "illegitimate transcription" (4) as an explanation of our results, as does the recent detection of TSH-R transcript in the salmon heart using a similar PCR technique (5).
We suggest that our differences from the study by Busuttil and Frauman (1) regarding TSH-R transcript in cardiac muscle tissue reflect the difficulties inherent in detecting transcripts of low abundance, namely the requirement for high-quality RNA prepared from fresh tissue, and for optimized primers and optimal PCR amplification conditions. In this context, we note that our RT-PCR studies were performed with poly A+ RNA (not total RNA) extracted from porcine cardiac tissues that were flash frozen in liquid nitrogen.
It remains to be determined whether TSH-R transcripts in the heart may have functional significance. Some evidence to this effect may be found in our subsequent studies with TSH-R expression and TSH activation of cAMP in human coronary artery smooth muscle cells in culture (6). However, a complete picture of TSH-R function in cardiac physiology will require additional studies to elucidate which specific cell types express this receptor, and how its expression might be altered in thyroid or cardiac diseases, as earlier suggested (7).
Received July 30, 2001.
References
This article has been cited by other articles:
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  B. E. Busuttil and A. G. Frauman TSH Receptor Expression in Cardiac Muscle Tissue J. Clin. Endocrinol. Metab., June 1, 2002; 87(6): 2994 - 2994. [Full Text] [PDF]
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 P. Glendenning, L. L. A. Laffer, H. K. Weber, A. A. Musk, and S. D. Vasikaran Parathyroid Hormone Is More Stable in EDTA Plasma Than in Serum Clin. Chem., May 1, 2002; 48(5): 766 - 767. [Full Text] [PDF]
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